Marine n-3 long-chain PUFA (n-3 LCPUFA) may have a beneficial effect on several aspects of the metabolic syndrome (dyslipidaemia, insulin resistance, hypertension and abdominal obesity). The metabolic syndrome is increasing in prevalence during adolescence, but only few studies have investigated the effects of n-3 LCPUFA in adolescence. The present study examines associations between fish intake (assessed by a 7 d pre-coded food diary), erythrocyte (RBC) DHA status (analysed by GC) and metabolic syndrome measures (anthropometry, blood pressure and plasma lipids, insulin and glucose) in 109 17-year-old children from the Copenhagen Birth Cohort Study. Of the children, 8 % were overweight or obese and few showed signs of the metabolic syndrome, but all the metabolic syndrome variables were correlated. Median fish intake was 10·7 (interquartile range 3·6–21·2) g/d. Boys tended to have a higher fish intake (P = 0·052), but girls had significantly higher RBC levels of DHA (P = 0·001). Sex and fish intake explained 37 % of the variance in RBC-DHA (P < 0·001). After adjusting for confounders, high DHA status was found to be significantly correlated with higher systolic blood pressure (P = 0·014) and increased fasting insulin (P = 0·018), but no adverse association was observed with the mean metabolic syndrome z-score. Overall, the present study showed the expected association between fish intake and RBC-DHA, which in contrast to our expectations tended to be associated with a poorer metabolic profile. Whether these results reflect the physiological function of n-3 LCPUFA, lifestyle factors associated with fish intake in Denmark, or mere chance remains to be investigated.

Increased intake of marine long-chain n-3 PUFA (n-3 LCPUFA) may decrease the risk of CVD and reduce mortality by lowering serum TAG and blood pressure (BP). Furthermore, n-3 LCPUFA may affect novel CVD risk markers related to inflammation and vascular function. The objective of the present study was to examine the effect of farmed trout on novel and traditional CVD risk markers in healthy men, and to evaluate whether this was affected by the aquacultural feed regime. We performed a parallel, 8-week intervention study in which sixty-eight healthy male volunteers were randomised to consume either a daily meal with 150 g farmed trout raised on either marine or vegetable-based feed, or a reference meal containing 150 g chicken. Twenty-four hour BP, pulse wave velocity, augmentation index, fatty acid composition of erythrocyte (RBC), and concentrations of TAG, HDL-cholesterol, LDL-cholesterol, glucose, insulin, C-reactive protein (CRP) and other markers of inflammation were measured at weeks 0 and 8. RBC content of total n-3 LCPUFA, both EPA and DHA, was significantly higher among men consuming trout raised on marine feed compared with men consuming the vegetable-fed trout or chicken. The three intervention groups did not differ significantly with respect to any of the other outcome variables, although there were trends towards associations between the changes in RBC n-3 LCPUFA and those in BP and CRP. In the present study, we conclude that we could not confirm the fish oil-induced reduction in CVD risk markers after daily consumption of trout with high or low n-3 LCPUFA content. However, trout raised on vegetable-based feed had less pronounced impact on RBC n-3 LCPUFA status.

The aim of the study was to characterize the time course of the development of high-fat diet-induced hepatic steatosis and its relation to body fat accretion and changes in plasma lipid profile. Female Sprague–Dawley rats were high-fat fed (HF; 42%, kJ) for 1, 2, 4, 6, 12 and 16 weeks and compared to standard fed rats (SD). Data obtained from HF rats were further analysed by classifying the animals into obesity-prone and obesity-resistant. In HF rats, liver lipid content increased rapidly by approximately 200% during the first 2 weeks, decreased almost to baseline levels between weeks 2 and 6, and re-increased by 17% between weeks 6 and 16 (P<0·05). Body weight, body fat accretion, plasma leptin, NEFA and glycerol concentrations were higher in HF than in SD rats (P<0·05). These higher values were established in 2 weeks and the differences between the groups did not further enlarge from weeks 2 to 16. Obesity-prone rats depicted higher body weight and body fat accretion than obesity-resistant and SD rats. Surprisingly, however, liver lipid content was the same in obesity-prone as in obesity-resistant rats as they were both higher than in SD rats (weeks 2 and 16; P<0·05). Our data support the hypothesis that the liver acts as a systemic buffer, largely increasing its lipid content in the early stage of high-fat feeding. Our results also suggest that the development of non-alcoholic hepatic steatosis is more linked to dietary fat ingestion than to body weight gain.